Antioxidants · 2 authors, 2 centres
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This narrative review discusses how iron dysregulation, leading to excess reactive iron, is a common underlying factor in a wide range of diseases, including infections, cancer, and neurological and inflammatory disorders. It reviews evidence that new therapeutic approaches targeting iron, such as improved chelators, hepcidin agonists, and ferroptosis induction, show promise for treating these conditions.
This narrative review synthesizes evidence that dysregulated iron homeostasis, characterized by excess free reactive iron, is a shared pathological mechanism in diverse human diseases. The review highlights that existing iron chelators have limitations, but new purpose-designed chelators and hepcidin agonists show promise in preclinical and early clinical studies for suppressing pathogen/cancer growth and alleviating iron-induced toxicity. Key limitations noted include the need to better understand whether iron dysregulation is a cause or consequence in many diseases. Implications suggest that therapies reducing excess labile iron could have broad applicability across multiple disease categories.
